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If you don't Yahoo, Here's a copy of the abstract about adie's and Lyme.
Margo
The Lancet
Volume 357, Number 9258
10 March 2001
Correspondence
Holmes-Adie syndrome and Lyme disease
Sir--Paolo Martinelli (Nov 18, p 1760)1 provides an excellent clinical and
historical overview of Holmes-Adie syndrome (tonic pupil and areflexia),
more commonly known in the USA as Adie syndrome. Although the syndrome has
not been associated with "infection of conventional bacterial or viral
origin", it is occasionally linked to early syphilis, parvovirus B19, and
herpes simplex virus infections.2-4 We now report an association with
neurological Lyme disease.
In a referral practice of about 140 patients with Lyme disease, we have seen
three patients with predominant neurological symptoms who presented with
Holmes-Adie syndrome (table). The diagnosis of Lyme disease was based on a
history of tickbite, presence of an erythema migrans rash and positive
serology for the spirochaete Borrelia burgdorferi. The duration of Lyme
disease symptoms ranged from 2-16 years, and each patient developed a
unilateral tonic pupil before the diagnosis of Lyme disease was made. All
three patients had significant neuropsychiatric and cognitive defects,
hyporeflexia, and facial dysaesthesia without anhydrosis. Rapid plasma
reagin testing was negative in each case. Two patients had abnormal brain
magnetic resonance imaging with white-matter lesions consistent with
neurological Lyme disease. A decreased concentration of CD57 lymphocytes
characteristic of chronic Lyme disease5 was found in two patients before
antibiotic therapy. Of note, Holmes-Adie syndrome persisted in each case
despite intravenous antibiotic therapy and partial resolution of other
neurological symptoms of Lyme disease.
Volume 357, Number 9258
10 March 2001
Correspondence
Holmes-Adie syndrome and Lyme disease
Sir--Paolo Martinelli (Nov 18, p 1760)1 provides an excellent clinical and
historical overview of Holmes-Adie syndrome (tonic pupil and areflexia),
more commonly known in the USA as Adie syndrome. Although the syndrome has
not been associated with "infection of conventional bacterial or viral
origin", it is occasionally linked to early syphilis, parvovirus B19, and
herpes simplex virus infections.2-4 We now report an association with
neurological Lyme disease.
In a referral practice of about 140 patients with Lyme disease, we have seen
three patients with predominant neurological symptoms who presented with
Holmes-Adie syndrome (table). The diagnosis of Lyme disease was based on a
history of tickbite, presence of an erythema migrans rash and positive
serology for the spirochaete Borrelia burgdorferi. The duration of Lyme
disease symptoms ranged from 2-16 years, and each patient developed a
unilateral tonic pupil before the diagnosis of Lyme disease was made. All
three patients had significant neuropsychiatric and cognitive defects,
hyporeflexia, and facial dysaesthesia without anhydrosis. Rapid plasma
reagin testing was negative in each case. Two patients had abnormal brain
magnetic resonance imaging with white-matter lesions consistent with
neurological Lyme disease. A decreased concentration of CD57 lymphocytes
characteristic of chronic Lyme disease5 was found in two patients before
antibiotic therapy. Of note, Holmes-Adie syndrome persisted in each case
despite intravenous antibiotic therapy and partial resolution of other
neurological symptoms of Lyme disease.
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